THE SILENT CORTICOTROPINOMA - IS CLINICAL-DIAGNOSIS POSSIBLE
THE SILENT CORTICOTROPINOMA - IS CLINICAL-DIAGNOSIS POSSIBLE
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DOI：
10.1007/bf03348769
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发表时间：
1992-06-01
影响因子：
5.4
通讯作者：
FAGLIA, G
中科院分区：
文献类型：
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作者：
AMBROSI, B;COLOMBO, P;FAGLIA, G
迄今为止，无症状促肾上腺皮质激素细胞垂体腺瘤的诊断仅依据组织病理学。在本文中，我们描述了6名妇女受垂体腺瘤，没有明显的临床特征的皮质醇增多症，其中的回顾性数据表明，在体内的临床诊断沉默的促肾上腺皮质激素瘤的可能性。所有患者的基础促肾上腺皮质激素和皮质醇水平均正常，低剂量地塞米松试验持续抑制血清皮质醇和尿17-羟皮质类固醇水平。CRH和/或赖氨酸加压素试验，在5例患者中进行，总是引起夸张的ACTH/皮质醇升高。在三个病例中，对阿片激动剂洛哌丁胺的反应进行了评估，没有发现ACTH/皮质醇水平的抑制。在5例促肾上腺皮质激素瘤的证据获得免疫组化或免疫荧光研究，此外，在一个腺瘤ACTH分泌到培养基中，在另一个CRH和精氨酸加压素诱导显着的细胞内[Ca++]上升。电子显微镜研究的腺瘤，从三个病人，显示存在腺瘤性促肾上腺皮质激素细胞。最后，在另一名妇女没有激素异常，最初观察到，她是一个“无功能”垂体腺瘤手术，但4年后，一个明显的库欣病出现，这表明一个沉默的促肾上腺皮质激素瘤随后成为功能，虽然形成一个不同的腺瘤不能排除。总之，ACTH/皮质醇对CRH和/或赖氨酸加压素的高反应性的发生，以及在明显“无功能”的垂体瘤患者中缺乏对ACTH/皮质醇分泌对阿片受体激动剂的抑制，可能允许在体内识别沉默的促肾上腺皮质激素瘤。
Up to now, the diagnosis of silent corticotroph cell pituitary adenomas has been made only on histopathological basis. In this paper we describe 6 women affected with pituitary adenomas, without evident clinical features of hypercortisolism, in whom retrospective data suggested the possibility of clinically diagnosing silent corticotropinomas in vivo. In all patients basal ACTH and cortisol levels were normal, and the low-dose dexamethasone test constantly suppressed serum cortisol and urinary 17-hydroxycorticosteroid levels. The CRH and/or lysine-vasopressin tests, performed in five patients, always induced exaggerated ACTH/cortisol rises. In three cases the response to the opiate agonist loperamide was assessed and no inhibition of ACTH/cortisol levels was found. All patients underwent pituitary surgery. In five cases evidence of corticotropinoma was obtained by immunohistochemistry or immunofluorescence studies; moreover, in one adenoma ACTH was secreted into the culture medium, and in another one CRH and arginine-vasopressin induced a marked intracellular [Ca++] rise. Electron microscopy study of the adenoma, removed from three patients, showed the presence of adenomatous corticotroph cells. Finally, in another woman no hormonal abnormalities were initially observed and she was operated for a "nonfunctioning" pituitary adenoma, but four years later an overt Cushing's disease appeared, suggesting that a silent corticotropinoma subsequently became functional, although the formation of a different adenoma cannot be excluded. In conclusion, the occurrence of ACTH/cortisol hyperresponsiveness to CRH and/or lysine-vasopressin and the lack of suppression of ACTH/cortisol secretion to opioid agonists in patients with apparently "nonfunctioning" pituitary tumors might allow the in vivo recognition of silent corticotropinomas.